Helicobacter

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Helicobacter
Helicobacter sp 01.jpg
Scanning electron micrograph of Helicobacter bacteria.
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Epsilonproteobacteria
Order: Campylobacterales
Family: Helicobacteraceae
Genus: Helicobacter
Goodwin et al. 1989
Species

H. acinonychis
H. anseris
H. aurati
H. baculiformis
H. bilis
H. bizzozeronii
H. brantae
H. canadensis
H. canis
H. cetorum
H. cholecystus
H. cinaedi
H. cynogastricus
H. equorum
H. felis
H. fennelliae
H. ganmani
H. heilmannii
H. hepaticus
H. mesocricetorum
H. macacae
H. marmotae
H. mastomyrinus
H. mesocricetorum
H. muridarum
H. mustelae
H. pametensis
H. pullorum
H. pylori
H. rappini
H. rodentium
H. salomonis
H. suis
H. trogontum
H. typhlonius
H. winghamensis

Helicobacter is a genus of Gram-negative bacteria possessing a characteristic helical shape. They were initially considered to be members of the Campylobacter genus, but in 1989 Goodwin et al. published sufficient reasons to justify his new genus name of Helicobacter | [1] The Helicobacter genus contains about 35 species.[2][3][4]

Some species have been found living in the lining of the upper gastrointestinal tract, as well as the liver of mammals and some birds.[5] The most widely known species of the genus is H. pylori, which infects up to 50% of the human population.[4] Some strains of this bacterium are pathogenic to humans as it is strongly associated with peptic ulcers, chronic gastritis, duodenitis, and stomach cancer. It also serves as the type species of the genus.

Helicobacter species are able to thrive in the very acidic mammalian stomach by producing large quantities of the enzyme urease, which locally raises the pH from about 2 to a more biocompatible range of 6 to 7.[6] Bacteria belonging to this genus are usually susceptible to antibiotics such as penicillin, are microaerophilic (optimal oxygen concentration between 5 and 14%) capnophiles, and are fast-moving with their flagella.[7][8]

Molecular signatures[edit]

Comparative genomic analysis has led to the identification of 11 proteins which are uniquely found in the Helicobacteraceae. Of these proteins, seven are found in all species of the family, while the remaining four are not found in any Helicobacter strains and are unique to Wollinella.[9] Additionally, a rare genetic event has led to the fusion of the rpoB and rpoC genes in this family, which is characteristic of them.[9][10]

Non-pylori Helicobacter species[edit]

Recently, new gastric (H. suis and H. baculiformis) and enterohepatic (H. equorum) species have been reported. H. pylori is of primary importance for medicine, but non-pylori Helicobacter species (NPHS), which naturally inhabit mammals (except humans) and birds, have been detected in human clinical specimens. NPHS encompass two (gastric and enterohepatic) groups, showing different organ specificity. Importantly, some species such as H. hepaticus, H. mustelae, and probably H. bilis exhibit carcinogenic potential in animals. NPHS harbour many virulence genes and may cause diseases not only in animals, but also in humans. Gastric NPHS such as H. suis (most often), H. felis, H. bizzozeronii and H. salomonis have been associated with chronic gastritis and peptic ulcers in humans and, importantly, with higher risk for MALT lymphoma compared to H. pylori. Enterohepatic species e.g., H. hepaticus, H. bilis and H. ganmani have been detected by PCR, but still are not isolated from specimens of patients with hepatobiliary diseases. Moreover, NPHS may be associated with Crohn's disease and ulcerative colitis. The significance of avian helicobacters (H. pullorum, H. anseris, and H. brantae) also has been evaluated extensively. NPHS such as H. cinaedi and H. canis can cause severe infections, mostly in immunocompromised patients with animal exposure. Briefly, the role of NPHS in veterinary and human medicine is increasingly recognised. Several other topics such as isolation of still uncultured species, antibiotic resistance and treatment regimens for NPHS infections and, last but not least, NPHS pathogenesis and possible carcinogenesis in humans should be evaluated.[2]

References[edit]

  1. ^ Goodwin CS, Armstrong JA, Chilvers T, et al. (1989). [doi = 10.1099/00207713-41-1-88 "Transfer of Campylobacter pylori and Campylobacter mustelae to Helicobacter gen. nov. as Helicobacter pylori comb. nov. and Helicobacter mustelae comb. nov., respectively"] Check |url= scheme (help). Int. J. Syst. Bacteriol. 39 (4): 397–405. 
  2. ^ a b Boyanova, L (editor) (2011). Helicobacter pylori. Caister Academic Press. ISBN 978-1-904455-84-4. 
  3. ^ Vandamme P, Falsen E, Rossaq R, et al. (1991). "Revision of Campylobacter, Helicobacter, and Wolinella taxonomy: emendation of generic descriptions and proposal of Arcobacter gen. nov". Int. J. Syst. Bacteriol. 41 (1): 88–103. doi:10.1099/00207713-39-4-397. PMID 1704793. 
  4. ^ a b Yamaoka Y (editor). (2008). Helicobacter pylori: Molecular Genetics and Cellular Biology. Caister Academic Press. ISBN 1-904455-31-X. [1]. 
  5. ^ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 0-8385-8529-9. 
  6. ^ Dunn BE, Cohen H, Blaser MJ (1 October 1997). "Helicobacter pylori". Clin Microbiol Rev. 10 (4): 720–741. PMC 172942. PMID 9336670. 
  7. ^ Hua JS, Zheng PY, Ho B (1999). "Species differentiation and identification in the genus of Helicobacter". World Journal of Gastroenterology 5 (1): 7–9. 
  8. ^ Rust et al. (2008). "Helicobacter Flagella, Motility and Chemotaxis". Helicobacter pylori: Molecular Genetics and Cellular Biology (Yamaoka Y, ed.). Caister Academic Press. ISBN 978-1-904455-31-8. [2]. 
  9. ^ a b Gupta, R. S. (2006). Molecular signatures (unique proteins and conserved indels) that are specific for the epsilon proteobacteria. BMC Genomics. 7:167.
  10. ^ Zakharova, N., Paster, B. J., Wesley, I., Dewhirst, F. E., Berg, D. E., and Severinov, K. V. (1999) Fused and overlapping rpoB and rpoC genes in Helicobacters, Campylobacters, and related bacteria. J Bacteriol 181: 3857-3859.

External links[edit]